Kitzmiller v. Dover Area School District

Trial transcript: Day 20 (November 3), PM Session, Part 2

Q. Thank you, Your Honor. Dr. Minnich, when you
were defining intelligent design earlier in your testimony you
noted the "deep complexity and clearly evident design in
organisms." Do other scientists recognize this complexity in
evidence of design?

A. Yes. All biologists see design in nature, and
this is really part of this central question, is it real design
or apparent design, and how do we differentiate between the two.
This is a cover of Cell again, this is our premier journal. From
a review issue, once a year they run a review issue, this is from
1999 I believe.

A. `98, okay, I can't remember, but macromolecular
machines, this dealt with the machines of life, and I think the
cover really sums it up. Across the landscape of biological
systems we find these incredible macromolecular machines.

A. Exactly. The entire issue is looking at
specific machines in the cell that we knew a lot about.

Q. And just I guess for purposes of the record
this cover can also be found as Exhibit 203-C, Charlie. I believe
another slide from an article that appeared in there in this
particular journal, this issue, from Bruce Alberts, is that
correct?

A. Correct. Bruce Alberts at the time was National
Academy of Science president. He's an evolutionist, so you know,
I don't want to misinterpret his position on any of this, but
it's an interesting article titled The Cell as a Collection of
Protein Machines: Preparing the Next Generation of Molecular
Biologists. Some of the things that he notes, the complexity of
the cell's macromolecular machines was not anticipated."

In the introduction of this article he states as a
graduate student in the 1960's they looked at the, you know,
cells that they were working on, E. coli at the time, as really a
bag of enzymes operating on the second order of kinetics, or
diffusion kinetics, "Our current view of the cell is vastly
different." In fact, he says, "We've always underestimated the
cell in this review." More complex than the view of the cell when
Dr. Alberts was a graduate student, okay, so I covered that.

Dr. Alberts advocates in this article
incorporating the principles of design engineering into biology
curricula for this next generation of molecular biologists as a
means to dissect the interactions of macromolecular machines now
identified in even the simplest cells. The point being that for
us to get to the next level of understanding at the cellular and
subcellular level, how all these molecular machines not only
function independently in and of themselves, but how they're
coordinately regulated as a consortium machines to carry out the
cell's duty will be the job more of the design engineer or a
systems analyst. These are true factories.

So I find it incredible. In fact, in the
acknowledgments he acknowledges Jonathan Albert, I don't know the
relationship, for the information in terms of how design
engineers approach these types of problems. We're going to need
this, you know, the age of cloning and sequencing is over, to get
to the next step. We're going to incorporate design
engineering.

Q. And again this article is marked as Defendant's
Exhibit 253, and I just want to verify if you look under Tab, I
believe it's Tab in your exhibit binder if you would, in the
black binder, if you'd verify this as the article you're
referring to?

Q. I believe you have another section from this
issue of the journal that you want to use to emphasize your
points?

A. Right. Can I just read one quote out of this
article, because again it's important to understand that Bruce
Alberts is an evolutionist. In fact, he's co-author of the book
on how to teach evolution at the secondary level, published by
the National Academy. But on the first page of this article at
the bottom, why do we call --

A. Correct, 253, on the first page. "Why do we
call the large protein assemblies that underlie cell function
protein machines? Precisely because like the machines invented by
humans to deal efficiently with the macroscopic world, these
protein assemblies contain highly coordinated moving parts.
Within each protein assembly intermolecular collisions are not
only restricted to a small set of possibilities, but retain,
reaction C depends on reaction B, which in turn depends on
reaction A, just as it would in the machine of our common
experience." So emphasizing that this is almost a definition of
purposely ordered parts that you find in Pandas and People or it
might be a used definition of irreducible complexity, highly
ordered parts that perform a function.

A. Correct. I think this is what I just read,
isn't it? Oh, no, this is actually from the table of contents for
this issue. "Again, like machines invented by humans to deal
efficiently with the macroscopic world, protein assemblies
contain highly coordinated moving parts. Reviewed in this issue
of cell are the protein machines that control replication,
transcription, splicing, nucleocytoplasmic transport, protein
synthesis, protein assembly, protein degradation, and protein
translocation, the machines that underlie the workings of all
living things."

Across the landscape again these are the machines
that are performing every function in the cell. Highly
sophisticated machines, many of which when we dissect them have
all the hallmarks of machines that design engineers have made in
our macro world. So again the inference, you know, we have the
question the appearance of design, is it real or just apparent?
We don't have a Darwinian mechanism to explain the appearance of
these in a step-wise manner. At the same time we do know from our
common experience, you know, cause and effect in the world, that
when we find these types of machines, they're the product of
intelligence, and these surpass anything that yet, you know, that
we can make ourselves. It's an inference, it's a logical
inference.

Q. I believe we have another slide with our
friend, the bacterial flagellum.

A. Right. Again this is my machine, and David
DeRosier at Brandeis University has done an incredible amount of
work on this. In a review article in Cell in 1998 he wrote, "More
so than other motors, the flagellum resembles a machine designed
by a human," all right? So there's question of design. As
biologists we all recognize it. It's a true rotary engine.

A. Yeah, I guess you would have to say, because we
have yet engineered a machine that can self assemble and
function, you know, actually have its own software written that
can call up and decide when and how many of these to make, where
to put them, etc. So it's incredible, I mean, when you look at
the parameters of this machine.

Q. And this, and again for reference purposes this
is from Defendant's Exhibit 274, and if you can just look in your
exhibit binder, I believe it's Tab 11, is this the article from
which you're quoting from?

Q. Now, you indicated these living organelles are
described as machines by you and by these scientists. Are they in
fact machines?

A. They are. I mean, again they have all the
components of a rotary engine. Rotor, stator, U joints, bushings,
drive shaft, that's how they're described, and by definition a
rotary engine has to have these components, regardless of the
scale. I want to point out, too, you know, just for the record
that we didn't know these things existed twenty or thirty years
ago this was the surprise.

Again emphasizing what Bruce Alberts says, our
conception of the cell has changed radically in the last twenty
to thirty years. In terms of how we view the cell he says that
we've always underestimated it, I have another quote here by some
colleagues, but I think it's perfectly legitimate to go back and
ask is natural selection mutation sufficient to prove or to build
this type of sophisticated machinery.

Q. But the bacterial flagellum isn't the only
machine in a cell, correct?

Q. And I believe you have some additional exhibits
to point out some other machines?

A. Yeah, I've included another rotary engine, the
ATPase we find in prokaryotic and eukaryotic cells. This is a
description of the torque generated in the transfer of this
energy to ATP synthesis. ATP is the energy currency of a cell, is
generated by oxidation reduction reactions in the cell, and
essentially what you do is you push protons across a membrane,
much like you would collect water behind a dam, and then you
bleed through ATPase, which acts as a turbine. For every third of
a turn, or 120 degree turn of this rotor, you generate
essentially one adenine triphosphate molecule.

The point being here I think is this group
conceded all, makes this point in their article in Cell that if
one ATP consumed for 120 degrees is one of, one may anticipate
from the make of this motor the efficiency of our ATPase is
nearly 100 percent, far superior to a Honda V-6. This is a direct
quote out of this article. So it's approaching 100 percent
efficiency in these machines that are being produced by the
random events and selection of Darwinian mechanism.

A. Yes, this is a cartoon, again it's a rotary
engine like the flagellar, it's a much smaller scale, but you can
see that you've got a stator here and a rotor with arem ATP is
generated as this turbine turns around up here.

A. Right, I think that's -- the fascinating thing
to me, and this is in part why I participated in this conference
in Rhodes in biomimetics is that engineers and architects have
recognized that biology, systems in biology have solved some
pretty complex problems, and when you consider nanotechnology,
the application of this, computer applications, pharmaceutical
applications, engineers are coming to biologists to learn about
these systems and how they may, you know, practically apply them.
So when you consider the bacterial flagellum, the speed at which
it rotates, the fact that it can, you know, reverse direction in
less than a turn, I mean that's like any time you have a machine
that can stop and start, it's the equivalent in machine language
of a one and zero. I mean, you can have that application in terms
of designing computers that are biologically based.

Q. Have you been asked to give presentations to
engineers about these molecular machines?

A. I have in my university, the University of
Idaho, I've given one talk to the physics department just based
on the bacterial flagellum as a nanomachine. They're interested
in the fluid dynamics of the system and how it operates at this
scale, and also to, I believe it was a mechanical engineering
department.

A. Yeah. So the other thing that I think caught us
by surprise is the sophistication of the information storage
system of the cell. DN A and RN A are really information systems
that store digital information just like our computers do. This
is out of a textbook, this is a genetic code that was solved in
the 1960's by Caron at Harvard and Nirenberg at the NIH, and
essentially you have as we all know from basic biology there are
four nucleotides that make up genetic information, and there are
twenty amino acids. It's combination of three of these letters
that determine each amino acid if this translation is occurring
between nucleotide language to protein language.

So for instance U in the first position, we call
this the five prime positions, the center position U, and U in
the third position codes for phenylalamine. UUC also codes for
phenylalamine. With four digits there are 64 combination. So we
have 64 three letter codons. Now, when this was determined in the
60's, so this is really the Rosetta Stone of genetics, when this
was determined in the 60's there was an intuitive recognition
that there seemed to be a bias in the code for amino acids that
if you had a point mutation, for instance if you have UUU and you
changed this last U to a C, you get the same amino acids.

So there's redundancy. UCU or UCC, UCA, UCG all
code for a series. You either get the same amino acid or a
similar amino acid in terms of its chemical properties. So that
was intuitively obvious. Now, if this is a product of arbitrary
chance and necessity, to quote Minot, then there's no reason that
this code is chosen over any other. Francis Crick referred to
this as a frozen accident. Carl Woese in his paper "Owed to the
Code" states that the genetic code has not evolved.

Now, with computer analysis we can actually look
at all of the random codes that can be generated. There are
millions of codes that can be generated with the parameters of
twenty amino acids and four nucleotide bases, and ask is there a
bias, is there a better code to minimize the effect of point
mutations, because that's really what we're seeing in this code,
and it turns that the natural code according to this author Hays
when this has been analyzed against millions of other arbitrary
codes is optimized to minimize the effects of point mutations,
okay, the very thing required to drive evolution.

We have a code that from the get go is optimized
to minimize the effects of point mutation. Now, that to me, and
my colleagues, too, when we've discussed this causes them to
pause. I mean, people just stop and get reflective. That to me
has a signature of design on it, okay, that you have a, this is a
sophisticated, this is the most sophisticated information storage
system that we know of. It's true digital code we've got, it
codes for algorithms.

Now we're talking about the cell working on fuzzy
logic, which is non-linear, which is much more complicated than
we considered in the past, and if this is a product of undirected
chance and necessity, I find that difficult, you know, that
nothing that Microsoft and Bill Gates's engineers yet have come
close to producing an information storage system like this.
That's what we're talking about in terms of design and looking
back. We didn't know about this system fifty years ago I mean,
when the code was broken in the 60's. Certainly Darwin didn't
know about it.

So you have this most sophisticated information
storage system coupled with macromolecular machines that are also
highly sophisticated, with ordered parts that we by definition
call are irreducibly complex, it's appropriate to go back and ask
is a Darwinian mechanism sufficient to account for the appearance
of these.

Q. You said that the DN A has been shown to resist
point mutations, is that correct?

A. It's not that it resists it, but if you have a
point mutation, which is common either in replication or just
exposure to the environment, perhaps mutagens or UV, light that
you can get a mutation in one of these codons, you know, to
convert a U to a C, or what we call a transition or a
transversion mutation, and often you'll get either the same amino
acid or an amino acid that's related in terms of its chemical
properties so that you don't disruption of that protein that's
produced with that mutational event. Now, it doesn't eliminate it
completely, but there is, we recognize that there is this bias.
This is optimized to negate the effect of point mutation.

Q. So it's optimized to negate point mutations
which are necessary for that selection to function?

A. I mean, that's -- Dawkins makes that argument
that because I can't imagine a mechanism that would produce this
that I suffer from incredulity, and I'm, darn it, you know, we
are trained to be skeptics. We are trained to look at things
through, you know, a very narrow lens. We're to be our own worst
critics, and it seems like in any other practice of science
that's how we operate, except when it comes to an explanation of
the origin of these systems, and then we're accused of being, you
know, suffering from incredulity because we can't imagine how
these came about.

We don't have the intermediates. Again for any
biochemical pathway we don't have the phylogenetic history for
any biochemical pathway or subcellular organelle. Yet as a
scientist I am supposed to accept this without blinking that this
is a product of a Darwinian mechanism, and I'm sorry, these are
highly sophisticated systems, and I know from experience that
when you see a machine, a rotary engine, in any other contest,
you would assume that there's an engineer around, and those are
the arguments that we're making.

Q. I believe you have another example, you
described the sliding clamp. Could you describe this?

A. This is DN A polymerase on the right, so this
is the copying mechanism for DNA replication. What I find
interesting, actually this was a paper that was given to me by a
colleague who we disagree with in terms, but he thought I'd be
interested in it. The clamp protein here, which forms this donut
around this double helix of DNA, in eukaryotic organisms or
higher organisms there's a dimer. We call it in yeast PCN A
protein.

In E. coli we also have a clamp protein, this is a
prokaryotic, a more primitive organism, it's a trimer. It's a
beta subunit of E. coli polymerase. Now, if we compare the
protein sequences that form this structure between E. coli and
yeast, we wouldn't pick them up as being similar in a computer
search. Now, this is, all organisms are required to replicate
their DN A. You would think that this would be a highly conserved
process by definition if prokaryotics eventually evolved
eukaryotes from some common ancestor, but what we find is a
protein that has almost an exact superimposable structure, one on
the other, forming the same function, but completely different
amino acid sequences.

This is a remarkable example of convergence, and
there are many examples of this coming out now at the molecular,
and as we'll talk about Simon Conway Morris says even at the
organismal level. We can't, at present we don't understand the
properties of protein folding, so we couldn't make a protein to
form this structure as a base for the assembly of the other
components of DN A polymerase. Yet we find in nature that this
has happened twice for the same function, the same structure, but
a different amino acid sequence. I mean, that's an incredible
finding.

Q. I believe you have another example, a gated
portal. Could you explain what this is?

A. The gated portal, so this is looking from the
nucleus of a eukaryotic organism, and I don't think it shows up
with that well on this slide, but this is a portal, or actually a
gate, so you have to have traffic material from the nucleus to
the outside, from the outside back into the nucleus.

These are proteins of nucleic acids, and we have
these gate systems or turnstiles, and we find that there's a very
sophisticated postal system in the cell that components of the
cell will have, you know, a molecular zip coding that will direct
them, first of all allow them to go through this portal, and then
afterwards direct them to their location wherever they're
required in the cell. That whole postal system of zip coding,
how, you know, a protein made of a cytoplasm is directed to the
membrane or to endoplasmic verticulum is an incredible area of
research and interest as well, and --

A. Correct, correct. So there's, you know, this is
a cross section of that. So here would be the nuclear membrane
and the components that have been defined by mutational analysis
that dictate what can come through or what can go back through
the nucleus. So proteins synthesized in the cytoplasm and in the
ruthear have to come back through if they're regulatory proteins
and interact with DN A. So there's a very important regulatory
system in terms of recognizing these proteins and directing them
to their locales.

Q. Dr. Minnich, it appears from your testimony and
sometimes from the prior quotes you have from other scientists
that our understanding of the complexity of life has, especially
at the molecular level, has probably advanced exponentially in
the last half century. Is that fair to say?

A. She's at Stanford. She's department chair in
developmental biology at Stanford, Changing Views on the Nature
of the Bacterial Cell from Biochemistry to Cytology. She would be
a contemporary of Bruce Alberts having gone through I think
graduate training in the 60's. So these people that are kind of
reaching retirement age are starting to reflect back on their
careers I think during the most fruitful research period in the
history of biology, and these are not uncommon statements.

So let me read what these two individuals say,
"How profoundly our view of the bacterial cell has changed since
we first started our lifelong fascination with life's smallest
creatures." They're both microbiologists. "Who would have
imagined that bacteria have proteins that assemble into rings,
that cluster at the poles of cells, that localize delocalize as a
function of the cell cycle, or that bounce off the ends of the
cell with a periodicity of tens of seconds.

"Who would have suspected that the origins
replication move to the poles of cells, that the machinery for
replicating DN A is stationary, and that it is the chromosome
that moves through the chromosome duplicating factory, or that
plasmas would jump from the cell center or the cell quarter
points following their replication." The point I just want to
make is that our view of the cell, even the simplest cell, has
changed profoundly, and we are, there are scientists that have
come through are, you know, awe struck in terms of the beauty and
complexity of the systems that we're studying.

A. Again the molecular machines that we find that
I work on were not anticipated, they weren't predicted. They have
the appearance of machines that engineers make. I'm going to
hammer this point home, but I think it's critical to understand
that we don't have a Darwinian mechanism for the step-by-step
intermediates to get there or build these machines, and we know
from definitional work on these machines that they're irreducibly
complex, and we'll go over that in the next section. But again
you take away one component, you trash the machine. That's how
you study them. That's how we figure out what the parts are in
each individual system that, you know, is our pleasure to work
on.

Q. I believe we have one last quote which I
believe we've seen already in this trial.

A. Right, from Mr. Dawkins and The Blind
Watchmaker. "Biology is the study of complicated things that give
the appearance of having been designed for a purpose." As
biologists we all see the design, and you can be like Richard
Dawkins and argue that it's only apparent design. If there is a
natural mechanism, a Darwinian mechanism, a variation on the
mutation that can produce it, I'm more reserved, I guess more
conservative and say, you know, to me it's real design, and it's
a scientific argument.

A. Okay. Our view of the cell is vastly different
from when Darwin's theory was first proposed, let alone our view
over forty years ago. The cell is now recognized as being orders
of magnitude more complex and sophisticated than Darwin
envisaged. While our understanding of the complexity of the cell
has increased by orders of magnitude, the mechanism to generate
the complexity, mutation and natural selection, has remained
constant, although there's some new avenues of research that I
find very exciting in this last part. It's reasonable to revisit
the question, again it's reasonable to revisit the question as to
whether natural selection is sufficiently up to the task of
design engineering this recognized sophistication we find in even
the simplest of cells.

Q. Do other scientists who are not intelligent
design advocates recognize the lack of an adequate Darwinian
explanation for this complexity in evident design?

A. I have a quote from Carl Woese in that paper
that was cited earlier alluding to this fact, and I don't think
I'm taking this out of context. "The creation of the enormous
amount of and degree of novelty needed to bring forth modern
cells is by no means a matter of waving the usual wand of
variation and selection. What was there, what proteins were there
to vary in the beginning? Did all proteins evolve from one
aboriginal protein to begin with? Hardly likely.

"Evolution's rule, to which there are fortunately
a few exceptions," which he doesn't give, "is that you can't get
there from here. Our experience with variation and selection in
the modern context does not begin to prepare us for understanding
what happened when cellular evolution was in its very early rough
and tumble phases of spewing forth novelty." All right, so Carl
Woese is saying essentially in these early stages of evolution,
whatever parameters were at work are not present today, which
again, I mean, bears on the question of doing the science.

I mean, there were conditions by admission perhaps
that we can't reproduce. You know, we've got to recognize that,
and I think it's important for students to recognize that, but
maybe the important thing here, evolution's rule to which there
are fortunately a few exceptions is you can't get there from
here. It means we can't, we don't have the intermediates to
account from how we got from the simple to the complex.

Q. And this article you're quoting from, if you
can again refer to your exhibit binder, Defendant's Exhibit 251,
and it should be I believe at Tab 5, is that the article you're
referring to?

Q. I just need to backtrack because I don't
believe we identified the exhibit number for the article from
Losick and Shapiro that you referred to previously, and I believe
it's at Defendant's Exhibit 257, which would be at Tab 10. Is
that the article you're referring to by Losick and Shapiro?

Q. Now, Carl Woese is not an intelligent design
advocate, is that correct?

A. Absolutely not. I mean, he's a well known and
like I said respected evolutionary biologist at the University of
Illinois.

Q. Now, we've been talking about Darwin's theory
of evolution. What's the common understanding of Darwin's theory?
I should say his principal contribution.

A. His principal contribution was the mechanism to
account for the variation that we see. So natural selection
coupled with variation, which from a neo-Darwinian perspective
once we understood genetic information was that mutation, natural
selection over time.

A. In terms can we demonstrate mutation and
selection? Yes. In terms of extrapolating that to larger systems
or going from, you know, the evolution of some of these machines
that we're talking about, we don't have the evidence.

Q. Are there gaps and problems with the Darwinian
theory of evolution?

Q. Is there a principal contention that you have
for the ability of this mechanism of natural selection to explain
the origin of life that concerns intelligent design?

A. Right, when you look at the origin of life
problem, yeah, I mean, you know, we don't, we can't reproduce it.
It's a lot of speculation.

Q. Let me perhaps rephrase that question because
it wasn't as clear as I wanted it to be. Is there a principal
contention you have with the explanatory power of the theory of
evolution that is particularly relevant for intelligent
design?

A. I'm not quite sure what you're getting at, and
other than the fact that we've got to explain, you know, these
machines which I say by definition are irreducibly complex.

Q. Can natural selection account for the origin of
these complex molecular machines?

A. Not at present. Again, we don't have the
mechanism. I think that natural selection can preserve them, and
this is in part I think where we may, you know, if I could look
at in a crystal ball and see a melding of these two ideas.
Natural selection is definitely a preservative. The question is
whether or not it's generative and if it can produce these novel
structures de novo, but certainly once these structures are
around it has a preservative effect, which is very, very, very
important in our study of biology.

Q. Well, can natural selection account for the
information storage systems required for the production of these
molecular machines?

A. No. No. We have no understanding in terms of
how nucleic acid information systems evolved, and in fact in our
chemical experiments, looking at primordial conditions we can't
get cytosine in all of the methods that have been tested to
date.

Q. How about do we have a phylogenetic history of
the single biochemical pathway for things such as the
flagella?

A. No. Again I think I stated this that, you know,
Jim Shapiro at the University of Chicago, Harold, a retired
microbiologist at Colorado State, says we don't have a single
phylogenetic history of a biochemical pathway or a subcellular
organelle.

A lot of conjecture, wishful thinking I think to
paraphrase their view.

A. Harold is a microbiologist, although Shapiro
has made similar statements. Jim Shapiro in an article that I
just read last week, a fascinating article, said there's no
contrivance of man that comes close to the simplest cell or one
of the subcellular organelles.

Q. Now, the theory of evolution, particularly
natural selection we've been talking about here, has it been able
to explain the existence of a genetic code?

Q. Can it explain the development of the pathways
for the construction of organelles such as the flagellum?

A. No. Like I said, we have to phylogenetic
history. I've worked on the bacterial flagellum for years and
there's to my knowledge not a paper that can tell me, you know,
the evolutionary assembly of this by a step-wise mutation
selection program, and we may never know it. That's the
problem.

Q. Is it fair to say that under this relatively
broad category of difficulties that we just went through lies
much of the structure and the development of life?

Q. And does this then cause you to question
whether a Darwinian framework is the proper way to approach such
questions?

A. That's why I'm testifying here. I mean it's
because of the scientific constraints I see in Darwinian
explanation.

Q. Some of the plaintiffs' experts have described
intelligent design as a science stopper. Would you agree with
that?

A. Absolutely not. I mean, turn it around. If you
just say, you know, like Woese, wave a magic wand of variation
and selection, where does that get you? You know, I think from my
own personal perspective, having something designed implies that
there's purpose and, you know, I can start teasing apart that
purpose and apply that in different ways, like a design engineer
or a systems analyst would approaching the machine where you
don't have the blueprints, you don't have the owner's manual, and
that's the beauty of it.

Q. So you're a working scientist, I mean you kind
of roll up your sleeves and go into laboratories and conduct
experiments quite regularly?

Q. And I'd like for you to explain that further. I
know you're prepared several slides to do that.

A. Okay, this is just a reiteration in terms of
how we function in the laboratory during the last half century,
we've gained a greater understand of biology at the molecular
level than the entire history of efforts in the proceeding
millennia, and I don't think that's an overstatement. The vast
inroads we have made in our understanding of the cell came by
techniques essential to a design engineer.

A. All right. I lost my place, let's see. Came by
techniques essential to a design engineer, not elements derived
from the theory of evolution. The mainstay technique of modern
biology has made use of the concept of irreducible complexity of
the cell's subsystems. And if I can have the next slide I'll
iterate on what I mean by that.

Q. This concept of irreducible complexity, that
was coined by Dr. Behe, is that correct?

A. Right, right, but I think any working molecular
geneticist recognizes that this really explains the approach that
we take. This is from Mike's, one of his publication, but I
co-opted it here, "By irreducibly complex I mean a single system
which is necessarily composed of several well-matched interacting
parts that contribute to the basic function and where the removal
of any one of the parts causes a system to effectively cease
functioning."

Q. Is this your understanding of the concept of
irreducible complexity?

Q. And I just want to know that this was from an
article written by Dr. Behe which has I believe already been
admitted as Defendant's Exhibit 203-H, for hotel. Is irreducible
complexity one of the, I guess one of the arguments or components
of the intelligent design argument, is that correct?

A. Right. And I find it difficult when, you know,
even this definition is challenged, whether or not it's real or
not, because to me as a geneticist this is really restatement of
Beadle and Tatum's principle back in the 30's, the two
individuals that got molecular genetics going in the last
century, you know. One gene, one enzyme, the idea you can use
mutational analysis to knock out as individual gene and produce a
phenotype, all right -- so if we can go to the next slide.

Q. Let me just ask you one question before you
move on. You have here in this definition, this system,
underlined, bold, and in capitals, what purpose was --

A. I think because often this is the part that's
misunderstood in terms of some of the people that debate these
issues, you know. It's not, we're not saying that you can't find
components of a given molecular machine associated with another
machine and another function. I mean, I have no problem with
microevolution co-opts and the certain parts, there are plenty of
examples like this.

The point being the system that's being studied,
the bacterial flagellum, if you take out one of the components of
the type three secretion system of the flagellum, we know that we
can build it, the cells don't move. That's not to say that you
can't have a type three system involved in another function in
the cell. But for the system that's being addressed it's
irreducible and complex when the fact that we've identified all
the components based on mutational analysis.

Q. Do you find that those who argue against this
concept of irreducible complexity change the definition to create
a straw man to knock it down?

A. You know, I don't know if I'd say straw man or
it's intentional. I mean, it's one way you can construe it, but I
think it's a subtle but important definition that we're talking
just about one system of the cell that we're addressing through
mutational analysis, and again you can have components that may
be similar in other systems that could be addressed separately,
but it's a key point.

Q. If you could, I know we have another slide for
this, break down for us this concept of irreducible complexity
and how you employ it in your work in the lab.

A. Okay. Molecular machines are comprised of a
core set of components that are arranged for a purpose essential
for function of that machine. If one of these components is
removed from the machine, there's a resulting overall loss of
function. If there's no function, then there's nothing to select,
you know, from a Darwinian perspective, or you have to assume
that there would be some selective advantage for an intermediate,
but this implies that mutations in genes encoding pieces of a
molecular machinery will yield selectable phenotypes based on
this loss of function.

A. Selectable phenotypes for a geneticist means
that you mutagenize these cells. The hard part for us is coming
with a screen or a selection to separate all the mutations that
have occurred from the ones that you want to study in the system
that you're interested in. I'll show you a picture of how this
works in the lab really simply to get this point across, but this
process of using mutagenesis and devising genetic screens and
selections to identify loss of function has yielded astonishing
findings over the last sixty years.

This is the bread and butter of molecular
genetics. If these systems we worked on weren't irreducibly
complex, we would know very little about them. This is a
mechanism how the fact that we want to identify all the
components of a given molecular machine, we make mutants that
trash the system, sort out, map the mutations, how many genes are
involved, and then start piecing it back together. It's a very
reverse engineering procedure more attuned to, you know, this
concept of intelligent design or reverse the design process to
understand how these systems work.

Q. Break down for us further this concept of
mutagenesis, and I believe you have a slide --

A. Sure. All right. I work on the bacterial
flagellum, understanding the function of the bacterial flagellum
for example by exposing cells to mutagenic compounds or agents,
and then scoring for cells that have attenuated or lost motility.
This is our phenotype. The cells can swim or they can't. We
mutagenize the cells, if we hit a gene that's involved in
function of the flagellum, they can't swim, which is a scorable
phenotype that we use. Reverse engineering is then employed to
identify all these genes. We couple this with biochemistry to
essentially rebuild the structure and understand what the
function of each individual part is. Summary, it is the process
more akin to design that propelled biology from a mere
descriptive science to an experimental science in terms of
employing these techniques.

Q. Do you have some examples employing this
particular concept of the flagella?

A. I do, in the next slide. Hopefully this will
cut to the chase and show you what we're talking about. This is
an organism that my students and I work on. This is a petri dish
about 15 millimeters size, filled with this soft auger food
source for the organism. It's soft in the sense the organisms can
swim in it, but it has some rigidity that they just don't slosh
around. Now, each one of these areas showing growth were
inoculated with a toothpick of cells, the wild type parent here.
So this is yersinia enterocolitica, a good pathogen, double
bucket disease if you ingest it.

A. Yeah, that's the center, okay? So it can swim.
So it was inoculated right here, and over about twelve hours it's
radiated out from that point of inoculant. Here is this same
derived from that same parental clone, but we have a transposon,
a jumping gene inserted into a rod protein, part of the drive
shaft for the flagellum. It can't swim. It's stuck, all right?
This one is a mutation in the U joint. Same phenotype. So we
collect cells that have been mutagenized, we stick them in soft
auger, we can screen a couple of thousand very easily with a few
undergraduates, you know, in a day and look for whether or not
they can swim.

Q. I'm sorry, just so we're clear on the record,
the two you're talking about on the bottom left, the first one
was the bottom left and the second one was the bottom right?

A. We have a mutation in a drive shaft protein or
the U joint, and they can't swim. Now, to confirm that that's the
only part that we've affected, you know, is that we can identify
this mutation, clone the gene from the wild type and reintroduce
it by mechanism of genetic complementation. So this is, these
cells up here are derived from this mutant where we have
complemented with a good copy of the gene.

One mutation, one part knock out, it can't swim.
Put that single gene back in we restore motility. Same thing over
here. We put, knock out one part, put a good copy of the gene
back in, and they can swim. By definition the system is
irreducibly complex. We've done that with all 35 components of
the flagellum, and we get the same effect.

Q. And those top left and the top right were
restored bacterial flagellum --

A. In this manner we've, in other labs, so this
would be a compilation of work done in a number of laboratories
around the world. We've contributed to part of this right here
and the front end up here, but this is a blueprint for building a
flagellum. You know, you have a master control switch that's
turned on when it's appropriate. To make a flagellum, turn on the
first set of genes, you lay down, you know, a base plate on the
inner membrane, and you start assembling from inside of the cell
out.

So we're putting in, you know, a drive shaft,
another ring, our U joint. There are checkpoint controls like
just in the assembly of any machine. If there's a defective part
there's a feedback loop that will shut down expression of all the
succeeding genes to conserve energy in the cell. Eventually you
have this rotary engine with a propeller that can extend about
five to ten lengths of the cell.

Q. So this is a blueprint of the flagellum that
was developed through using this mutagenesis technique that
you're referring to?

A. Right. That and biochemistry and cell biology,
I think David DeRosier's done a lot of work with the mutants, you
know, showing their assembly. You get these, we call them
rivet-like structures. So different mutants you can actually
isolate these structures at various stages.

Q. Would it be accurate to say then the design
principle which I believe you referred to them as work because
these systems are irreducibly complex, is that correct?

A. By definition. Again, you know, this is how we
do this type of work.

Q. Now, there are some scientists, and Dr. Miller
is one of them, that claim that the bacterial flagellum is not
irreducibly complex, and he'll point to the type three secretory
systems to make his argument. Are those arguments correct?

A. I think they were a valid argument when they
first came out. In fact, we worked on type three secretion
systems. So when we're talking about that, this structure over
here on the right side of this slide, this is an electron
micrograph, this is essentially a micro or a nano syringe for the
plague organism, like I said, this has killed two hundred million
people alone, and most Gram-negative pathogens have them.

We were working on the regulation between motility
in yersinia enterocolitica and expression of virulence genes
which involved a subset of these proteins back in the early 90's,
and in fact we made the hypothesis that the toxins made in this
system, we didn't know about type three secretory systems at the
time, actually using Occam's Razor would be the flagellum. I
mean, we had good genetic evidence that the flagellum could be
used for other than secretion of flagellar proteins, but there's
a subset of proteins involved in both of these at the base that
dictate what proteins are secreted through these structures.

You build a flagellum from the inside out, all the
components are transported through this hollow core and assembled
at the distal tip, and with this nano syringe you make toxins and
they're actually injected into your white blood cells when you
make contact. They're a subset of common proteins between those,
and so after reading Mike's book I actually corresponded with him
and said, you know, we may have an intermediate for the
flagellum.

That's a possibility based on our early studies of
this. These structures were identified in 1998 by electron
microscopy finally, and Dr. Miller, Ken Miller has said that
these are the intermediate structure for flagellum biosynthesis,
and I was willing to entertain that view. But since then our own
work and work in other laboratories I think is showing that it's
actually the other way around, that the type three system if
anything has been derived from he flagellum. In one of my papers
I make that argument. So really to explain this structure you
have to presuppose the very thing you're trying to explain. In
fact it's being derived from a more complex system.

A. By definition I mean all the components for the
type three system were identified by mutational analysis, and in
this case attenuation of virulence.

Q. Would it be fair to say that if the type three
secretory system was found to have preceded the bacterial
flagellum, we'd still have difficulty with trying to determine
how that one system that functions as a secretory system could
then become a separate system that functions as a motor,
flagellar motor?

A. Right. I mean, that would be a positive
argument, I mean, in the sense that it could be an intermediate.
But again I think the evidence is falling heavily against it. But
sure, but having a nano syringe and developing that into a rotary
engine, you know, is a big leap.

Q. You wrote a paper, and we showed it up here on
this next slide, they referred to previously, "The Genetic
Analysis of Coordinate Flagella in Type Three Regulatory Circuits
and Pathogenic Bacteria," and I believe it's listed as
Defendant's Exhibit 254, which should be under Tab 8 in the
exhibit binder. If you can confirm that that's the article?

Q. Could you explain a little further this
article, its findings and its implications for intelligent
design?

A. Again it's a review of the reason, you know,
that we've teased out why pathogenic organisms regulate
production of a flagellum in a host environment, and they switch
between these type three systems. We show in this paper that
there is a logical reason for this, because if you operate these
systems simultaneously, in other words if we artificially express
flagellum protein, which makes up the filament of the flagellum
in the host environment, it will be recognized and secreted by
that nano syringe.

In fact, will be injected into a white blood cell.
Since over the last three to four years we've come to recognize
that the sentinel cells of our innate immune system, white blood
cells, neutrophils, dendritic cells, have on their surface a
receptor looking for bacterial flagellum as a pattern recognition
molecule of an invader, and if that receptor gets tickled with
flagellum it will induce the innate immune response and an
inflammatory response.

So the whole point I think it comes into play is
why a lot of organisms shut off motility in the host environment
is to hide this protein from invading cells, or from the sentinel
cells, the white blood cells, that they're going to encounter.
That has lots of ramifications. It explains yersinia pestis, the
bubonic plague organism, is nonmotile even though it has residual
flagellar genes in tis chromosomes.

Flagellar dysentery, the organism that causes
bacterial dysentery, has flagellar genes in its genome, but it's
nonmotile. Bordetella pertussis, which we were all immunized for
as kids, whooping cough, has flagellar genes in its chromosome,
but it doesn't express them because they all operate type three
systems. The point being if the type three system is going to be
an intermediate, there would be to have sometime in their history
where they would both be operational, and that would really work
against the organism.

I'm going into detail and I don't want to bore
people with it, but I find it, you know, fascinating that these
important pathogens have lost flagellar synthesis over time, and
there's a reason for it in terms of this. We're actually taking
purified flagellum, knowing this interaction and why it's
dangerous to expose white blood cells to flagellum. We can take
purified flagellum, expose a mouse by aerosol or internasal, and
the next day challenge it with ten lethal doses of yersinia
pestis or francisella tularensis, which causes tularemia, and it
shows significant delay time to death or even protection. I mean,
this has been, this is really going to change things in terms of
how we look at the initial stages of disease --

THE COURT: Oh, you're not boring me, but I'm
concerned about his ability to get -- Wes of course drew the
short straw in the court reporter pool for the afternoon, and I'm
just concerned that Wes got that. You're going to have to, when
you get to a term, what my concern is when you get to a term like
several of the terms to try to spell that. Not to protract
things, but --

Q. If you could go back, you mentioned several
diseases and bacteria. If you could restate those perhaps spell
to help us out. The disease for the whooping cough and some of
the others that you've mentioned.

A. Okay, in terms of you yersinia,
Y-E-R-S-I-N-I-A, pestis. That's the bubonic plague organism.
Shigella, S-H-I-G-E-L-L-A, bordetella, B-O-R-D-E-T-E-L-L-A, so
these are all organisms that operate type three systems that have
lost the ability to make a flagellum over time. But the point I'm
trying to make is that by approaching this kind of in a systems
analysis way it suddenly make sense why organisms regulate these
systems, why they're not displaying those proteins, and then we
can take advantage of this in terms of our understanding of the
innate or nonspecific immune response and manufacture really
novel vaccines. New adjuvants, we can use flagellum, you know,
packed with epitopes for plague or tularemia or other organisms,
and --

A. Right, T U-L-A-R-E-M-I- A I think. I almost
have to see it to write it. From Tulare County. Okay, so the
point being that this has all kinds of applications in our own
work.

Q. And so you, by looking at this from our
perspective of real design you're finding a great deal of utility
in applying that approach to it in terms of actually perhaps
providing some antibodies or some way to resist these things that
will be beneficial to, beneficial results for the community?

MR. HARVEY: Objection. Leading. I think he's
summarizing a lot of testimony. He's not developing the testimony
or moving it along there, which I wouldn't object to, because it
does tend to move things along. I think he's testifying, and
that's not proper when you've got your own witness, particularly
an expert witness, who should be able to explain.

MR. MUISE: Your Honor, it was an attempt to
summarize, we had some fits and starts with the spelling of these
bacteria, and it was just an attempt to summarize --

THE COURT: I think -- it's a close call, but I
think it's a fair summary at this point. I understand the point.
So I'm going to overrule the objection. You can proceed.

A. Yes, I agree. I think, you know, going back to
Bruce Alberts that we're looking at this thing kind of from the
systems perspective and --

Q. Dr. Minnich, another complaint that's often
brought up, and plaintiffs' experts brought it up in this case,
is that intelligent design is not testable. It's not falsifiable.
Would you agree with that claim?

A. No, I don't. I have a quote from Mike Behe. "In
fact, intelligent design is open to direct experimental rebuttal.
To falsify such a claim a scientist could go into the laboratory,
place a bacterial species lacking a flagellum under some
selective pressure, for motility say, grow it for ten thousand
generations and see if a flagellum or any equally complex system
was produced. If that happened my claims would be neatly
disproven."

A. It could be, and I, you know, would say that,
you know, up the ante. I'll give somebody a time three secretory
system intact and the missing proteins required to convert it
into a flagellum and let them go, see if you can get a flagellum
from a type three system. That's a falsifiable doable experiment.
That's just the type of experiment that could be subjected to
this type of analysis.

A. You know, I think about it, I would be
intrigued to do it. Knowing the tolerance limits for these
proteins and how they would assemble I wouldn't expect it to
work. But that's my bias.

Q. You think natural selection could account for
that, take the type three secretory system, the additional
proteins, and see if natural selection can build a bacterial
flagellum from that?

A. I'm not convinced that it could, but again it's
a plausible experiment. They should write a grant and see if we
can do it.

Q. One of the examples that had come up in the
course of this trial and I know you're somewhat familiar with,
you addressed it in your expert report, it's listed "Icon of
Evolution: Antibiotic Resistance." Is this a good example of
evolution in practice?

A. Because it really, it's an extrapolation from
the data. It's a good example of adaptation, you know, and here
I'm talking about point mutations conferring resistance to
specific antibiotics like streptomycine, which is commonly used
as a demonstration. You can show a population of cells are
sensitive to this drug, put them under selective pressure,
isolate mutants that are resistant. It comes with an extreme
fitness cost.

You know, from my own experience in this you can
almost, almost a doubling of the generation time required. These
organisms have a difficult time competing. Once the selective
pressure is removed you can get compensatory mutations, and this
has been shown in the literature, that restore the growth rate,
but only for the conditions in which you're doing the
experiments.

In actuality in biology we have a term for this
referred to as Mueller's Ratchet, and that essentially says that
when you have a mutation that you turn the ratchet once you're
limiting the organism's ability to respond to the next
environmental condition required for an adaptational response.
And so the more environmental insults or mutations that occur,
you're turning this ratchet down tighter and tighter to the point
where you're going to limit the organism's ability to eventually
survive.

So you can show this in this laboratory, it's a
beautiful demonstration of adaptation in mutation, but to
extrapolate this to the general principles of going from the
simple to the complex I think it's out of bounds. If anything
it's showing limits or the shortcomings of mutation. I don't
think it has anything to do with the complexifying mutations
required to drive evolution.

Q. And do scientists other than intelligent design
advocates recognize this?

A. Yes. This was in the literature. I can go back
and look at this paper by Simon Conway Morris, again this is a
paleontologist at Cambridge University, well known, this article
titled Evolution: Bringing Molecules into the Fold, you know,
this is the one where he says that he's going to do this perverse
thing about addressing the problems in evolution in the abstract,
and he goes through the problems that we have. We cannot still
differentiate phenotype from genotype.

In other words, the outward expression, the
morphology of an organism from its genome, we have a problem in
terms of phylogenetic assignments and looking at phylogenetic
histories, related histories of derived from molecular clocks
versus the fossil record. They're out of sync. Molecular clocks
tend to indicate the organisms are much more older than fossil
record. The paleontologists argue their interpretation is
correct. Molecular biologists will argue that their
interpretation is correct.

This has to be resolved. When we look at molecular
data we get conflicting phylogenies. If you compare a cytochrome
amino acid sequences, which was done back in the 60's and the
70's, compared the ribosomal RNA sequences, compared the
superoxide dismutates, other essential conserve genes or proteins
in the cell, you'll generate a different phylogeny depending upon
whether you're looking at one individually or in combination, and
this is now being superseded by comparing entire genomes.

So bioinformatics is going to be critical in this
next stage. You have this question of convergence that we
mentioned before again with a beta protein, beta subunit of DN A
polymerase, Morris remarks in a couple of examples in this paper
and even says if evolution is channelled, in the sense that it's
always coming up with the same solution being different routes,
pretty complex problems, in his mind teleology is back on the
table for discussion.

Now, this is a paper in Cell, and he says it's
interesting that physicists are reaching the same conclusion in
terms of the anthropic principle or the fine tuning principles of
the universe. He cites Barrow and Tipler, one of which is a
design proponent. As physicists he also cites a reference in
terms of biology of Michael Denton, who has been involved in
intelligent design and wrote a book previously to the one cited
in this article, Evolution: A Theory in Crisis. So here you have
a well known paleontologist looking at the problems of evolution,
recognizing that they're real, and considering maybe this word
teleology, purpose, should be back on the table for
discussion.

Q. Dr. Minnich, I'd like you just to sort of
summarize some of these points that you've been discussing
here.

A. I think if you look at the Carl Woese's paper
and read it carefully, he says that nothing in evolution should
be not subject to intense review. He even says common descent was
a conjecture, an idea of 19th century biologists, that somehow
got set in stone. We shouldn't be stuck to it. But I think in
terms of my experience, we're dealing with dogmatism versus
science and where the data is leading us.

Again to emphasize, we can't differentiate
genotype from pheno. I read a paper last week, you know, one of
the best phylogenetic histories we have is fossil horses in North
America. These have been, you know, from the Pleistocene and
Miocene time period, and I'm not a paleontologist, but I'm
interested in the molecular analysis. These have been well
characterized in terms of their phylogenetic history and
taxonomy, molecular techniques, isolation of fossil DN A
comparing to mitochondrial sequences shows that this phylogeny is
artificial, that they're all in the same taxa, perhaps even in
the same species.

It can't explain the origin of information. This
is still a major question in biology, and we're dealing with the
most sophisticated information storage system that we know about.
We can't explain how life initiated. Origins. We can't explain
the existence of the genetic code, this frozen accident I
referred to. Convergent examples in evolution are causing people
to question, and this is at the molecular level, the organismal
level.

So I would say that quoting Tulkinghorn, we're in
a situation much like the physicists were at the end of the last
century, and we suffer from this triumphal arrogance where we
think everything can be explained by our Darwinian methodology,
just like physicists, everything can be explained in Newtonian
mechanics. I think we're at a turning point, and that's not to
say that all the work before is not valuable. I think it's
critical. I think -- I love reading evolution, and these are
important contributions to understanding of life, but I'm
convinced there's something more there, and that's why I'm
here.

Q. Dr. Minnich, I want to sort of shift our focus
a little bit and talk a little bit about creationism. Is there a
popular understanding of this term?

A. Creationism has to deal with viewing scientific
or the empirical evidence through a literal interpretation of
Genesis, six-day creation event.

A. Again these are scientists that are limiting
how they interpret the data through a scriptural context of
Genesis, a literal interpretation of Genesis.

Q. Plaintiffs countering that intelligent design
is not science but rather creationism, are they correct?

A. No. We have don't have any precommitment to any
scripture, revelation, religion. Just looking at the empirical
data and using scientific, standard scientific reasoning of cause
and effect and asking is it real design or only apparent
design.

Q. Dr. Miller made a claim that if the bacterial
flagellum was designed, then it had to be created and therefore
it was special creationism. Is that accurate?

A. I don't agree with that. I mean, it doesn't say
anything about how it was designed, over what time period it was
designed, how it's been modified, you know, over time in terms of
evolutionary events. So I would disagree.

Q. Could the bacterial flagellum be designed over
time under intelligent design theory?

Q. Towards the bottom and then continuing on to
the next pages it says, "Intelligent design means that various
forms of life began abruptly through an intelligent agency with
their distinctive features already intact. Fish with fins and
scales, birds with feathers, beaks, and wings, etc., " and it
goes on to say, this is the next page, "Some scientists have..."
--

Q. Let me read this again for you again.
"Intelligent design means that various forms of life began
abruptly through an intelligent agency with their distinctive
features already intact. Fish with fins and scales, birds with
feathers, beaks, and wings, etc." And it goes on to say, Some
scientists have arrived at this view since fossil forms first
appeared in the rock record with their distinctive features
intact and apparently fully functional rather than gradually
developing." Do you see that?

Q. Does this statement in Pandas that I just
reviewed with you, does this make intelligent design
creationism?

A. No, I don't think so. I mean, this is a literal
interpretation of the fossil record where you see the sudden
appearance of these forms, you know, fish with fins, etc. in a
geologic record. From my interpretation this isn't ex nihilo, you
know, creation from nothing.

Q. Are you familiar with other scientists who are
not intelligent design advocates making statements regarding the
fossil record using the term abrupt appearance?

A. Right. I mean, this is common in paleontology
literature. From my understanding Woese even talks about it in
the one paper saltational events.

THE COURT: Well, the objection is that he's not
qualified. Tell me why he is. Tell me where it's in his report.
Tell me -- it's a technical objection, but it's an objection
that's founded in the lack of qualifications.

MR. MUISE: He's testifying about the book, Your
Honor. That's what he's, about it being good for science, and he
said so in his report. He used the term, all I asked him was the
term about saltational events and what did he mean by saltational
events. He's familiar with the literature. He cited from Carl
Woese's article. Carl Woese is a person he's been relying on in
most of his testimony.

THE COURT: All right. That's your argument. I'll
sustain the objection. You'll have to ask a different
question.

Q. Now, in your deposition you claim that the NAS
A SETI project, which stands for the "Search for Extraterrestrial
Intelligence," that that program was seeking a supernatural
explanation by searching for intelligence from space. Do you
recall that?

Q. In what sense were you using supernatural to
describe these explanations?

A. I think in my deposition I made it clear that
these were above our normal experience, or natural experience. So
I categorized them as if they're are not natural to our
experience they would be supernatural in that limited sense of
the word.

Q. Is it not true that from a scientific
perspective these explanation are actual natural
explanations?

Q. We heard quite a bit of testimony during the
course of this trial about methodological naturalism, and I
believe you indicated in your deposition you see that as placing
limits on intelligent design, is that correct?

A. It does. It can. In the sense that it limits
explanations it can be advanced, but it has the same kind of
stricture on other avenues of scientific research as well.

Q. Does methodological naturalism necessarily
exclude intelligent design from the realm of science?

Q. I'd like to read that to you here in a moment.
This is a statement read to the students from the January 2005.
"The Pennsylvania academic standards require students to learn
about Darwin's theory of evolution and eventually take a
standardized test of which evolution is a part. Because Darwin's
theory is a theory it continues to be tested as new evidence is
discovered.

"The theory is not a fact. Gaps in the theory
exist for which there is no evidence.

A theory is defined as a well tested explanation
that unifies a broad range of observations. Intelligent design is
an explanation of the origins of life that differs from Darwin's
view. The reference book Of Pandas and People is available for
students who might be interested in gaining an understanding of
what intelligent design actually involves.

"With respect to any theory, students are
encourage to keep an open mind. The school leaves the discussion
of the origins of life to individual students and their families.
As a standards driven district, class instruction focuses upon
preparing students to achieve proficiency on standards based
assessments." Sir, did I read anything to you in that short
statement that in your expert opinion will cause any harm to a
student's science education?

Q. Dr. Alters, who testified on behalf of the
plaintiffs, made the following comments about in his opinion the
effect or impact of this statement. I want to read you from his
testimony, and he's referring to this, the statement I just read
to you. "Now, what this policy is doing is saying that there's
this other scientific view that belongs, it belongs in the game
of science, and it's the one that most students will perceive as
God friendly. It has an intelligent designer. Evolution
doesn't.

"Now students are going to be in there discussing
out on the playground, discussing in their class, among
themselves or whatever, that the unit that they're now about to
hear about, the evolution unit, that's now coming up is the one
that's not God friendly, the one scientific theory that doesn't
mention God. But this other so-called scientific theory,
intelligent design, is God friendly because there's a possibility
that God has this other theory.

"What a terrible thing to do to kids. I mean, to
make them have to think about defending their religion before
learning a scientific concept, how ridiculous. This is probably
the worst thing I've ever heard of in science education." What's
your reaction to that those comments?

MR. HARVEY: Objection, Your Honor. Outside the
scope of his expert report. He didn't submit an export report in
rebuttal to Dr. Alters' report. No mention of the statement in
the expert report. I don't think it's proper.

MR. MUISE: Your Honor, it's all in line with why
he believes this is good science education. We've had one expert
making these claims, and I'm asking him to comment on those
claims as part of his opinion to demonstrate why this should be a
part of science education. This was testimony from trial. To say
he didn't have it in his expert report is --

THE COURT: Well, I understand that. That begs the
question, the question has been raised by Mr. Harvey's objection
is, is it in his export report. I do not believe it is. I think
you can probably concede that point. Obviously it can't be
because the report was prepared prior to Dr. Alters' testimony.
Now, the objection then states that there's no rebuttal report
that contains this. So in effect he's claiming I think that he's
not qualified, and surprised. What do you say about that?

THE COURT: I know exactly what he's testifying
about. Don't reiterate what he's testifying about. Tell me why I
should allow the testimony based on the fact that it's not in the
report and that it's, well, fundamentally not in the report, and
I think there's a qualification objection inherent in this that I
allowed Mr. Harvey to reserve. Dr. Alters in his testimony could
take this one step further, he's qualified in that area to render
that opinion. Was he not?

MR. MUISE: Dr. Minnich is also rendering an
opinion that he's qualified regarding this particular policy at
issue and whether intelligent design is science and whether it's
beneficial for the students.

THE COURT: No, that makes no sense what you just
said. Dr. Alters was qualified prior to his testimony on the
subject of, in the realm of whether he could testify as to
whether or not this was good practice to read this statement to
9th grade students. Now, I understand the purposes of this
witness generally, but you haven't qualified him on that point.
It's on education, and --

MR. MUISE: I'm saying you accepted him for science
education. Is that --

THE COURT: I accepted him subject to, don't
misunderstand what I said, subject to objections by Mr. Harvey.
Now, the objection goes generally to qualifications and -- it
goes broadly to qualifications, but it goes precisely now to a
statement outside the report. Now, you had the ability, and in
fact you have the obligation if he's going to render an opinion
in this area to supplement the report and you didn't do that. So
strictly speaking it appears to me to fall considerably outside
the report. He may have an opinion on this, I understand that,
but it's both outside the report and it's both that and not
within the qualifications as I perceive them to be. I also said
if you lay a foundation I might consider it. There is no
foundation for the opinion, and therefore the objection is at
this point sustained.

Q. And essentially if I understand your
contention, it is that an irreducibly complex system is one in
which it cannot function unless all the parts are there, and you
take away one part and the system ceases to function,
correct?

Q. And the point that you're trying make for
purposes of evolution is that irreducibly complex systems in your
view cannot evolve?

A. I think it's a problem for evolution. In other
words, for each intermediate part you have to have some selective
advantage to that intermediate structure, and that hasn't been
demonstrated. We know that if you remove one part you have no
function, and then if you have no function you've got nothing to
select.

Q. You didn't originate this idea of irreducible
complexity as a problem for evolution, did you?

A. No. I think Mike Behe coined the term, but
underlying is the basic argument of design is to account for
these complex structures that we find in nature to have the
appearance of design, is it real design or apparent.

Q. Well, and in support of your argument today you
spent a certain amount of time with pictures of what you called
motors. Did I understand that correctly?

Q. Well, I'd like you to go to pages, there's page
numbers in the upper, in the corners, in the upper corners, and
I'd like you to look at pages 16 to 21. I'm not going to ask you
to read it, but I'd just like you to look at it and see -- Matt,
if you could page through beginning with page 16 to 21, we'll go
through it, I'll invite you to read it if you'd like to, but if
you see on page 16 there's a section that begins "bacterial
motility"?

Q. And then on the next page if you turn the page
you'll see, Matt, if you can just highlight the language in the
lower right-hand column? Yeah, right there, the words "bacterial
flagellum," and it's a description of the bacterial flagellum in
this piece of literature from this creation science organization,
and then if you turn the page again to page 18, there's a
description there of the bacterial flagella rotor. Can you
highlight that lower paragraph there, Matt? And you'll see it
says, "As resolved by electron microscopy, it consists of a
series of flanges, grooves, and wheels, yes, wheels, mounted on
an axil and turning on bearing surfaces with an efficiency that
would be the pride of any industrial research and development
operation." Do you see that?

Q. And then if you'd just please turn the page one
more time, there's a diagram, and it's actually Figure 9 in this,
and Matt, if you could blow up Figure 9? You have to go to the
next page. I'd like the language at the bottom, please. And then
if you could, would it be possible to put up Dr. Minnich's slide
18?

Q. And I'd like to ask you just to look at that.
Do you see on the Figure 9 from this creation research society
publication that there's a picture of the motor rotor complex of
the bacterial flagellum?

Q. And then if you look to the picture that's in
the creation research society publication, you'll see that
there's, that that diagram has a universal joint as well. Do you
see -- actually if you look at the bottom and the language at the
bottom.

Q. And then there's something called, in this
Plaintiff's Exhibit 853 there's something called a stationary
ring, and in yours you have, also have something in that same
place, except it's called an "S" ring, is that right?

Q. Now, and if you turn to page to the next
page of this publication, on page 20 -- Matt, can you bring this
up? On the left-hand side of the page, about one-third of the way
down there's a reference there to bacterial nanomachines. Do you
see that?

Q. And then here's where the claim of
essentially what I believe is irreducible complexity comes in, if
you look on the right-hand side of the page it says -- it's
actually the first full sentence on the right-hand side
underneath the diagram, it says, "However, it is clear from the
details of their operation that nothing about them works unless
every one of their complexly fashioned and integrated components
are in place." Do you see where it says that?

Q. And then finally, and I'll bring this to
a close, if you go to the abstract on the page, page 13? Matt, if
you could just highlight the second half of that, beginning with
the word "in terms of biophysical complexity"? I'll read it to
you, it says, "In terms of biophysical complexity, the bacterial
rotor flagellum is without precedent in the living world. To the
micromechanician of industrial research and development
operations it has become an inspirational, albeit formidable
challenge to best efforts of current technology, but one ripe
with potential for profitable applications. To evolutionists the
system presents an enigma. To creationists it offers clear and
compelling evidence of purposeful intelligent design." Do you see
that?

Q. I did it again, I'm sorry. I'll just ask
the court reporter just when he hears that to just put in
Minnich. I'd like you to agree with me, to know whether you agree
with me that that is the same argument that you have advanced
here today in your direct testimony.

A. Right, I mean in terms of -- I don't have
any problem with that statement. And I would add that Howard Berg
at Harvard University refers to the bacterial flagellum as the
most efficient machine known in the universe. So across the board
whether, I don't -- what are we arguing here?

Q. I'm just, you're just confirming for me,
and I think you just did, that what we have just reviewed in this
Plaintiff's 853 is the, precisely the same argument that you
advanced today in support of your, in your direct testimony,
isn't that correct?

A. Yeah, in essence I mean I don't disagree
with you. If you're trying to make a connection with creationism
though I would disagree.

MR. HARVEY: Well, let's take a look at
another exhibit. Could you please go in your binder to what's
been marked as -- Your Honor, am I going to be able to run over
for a few minutes? Because if not I might as well stop.

THE COURT: Why don't we -- Wes has been out
here a while, because we've had an extended second session this
afternoon because we started early, so I think this would
probably be a good time to break. We'll invoke the mercy rule for
Wes's benefit because of a lot of complicated testimony this
afternoon. All right, you're going to be able to wrap up
obviously it would appear to me your cross and any redirect
comfortably within the morning tomorrow?

THE COURT: All right. Let's try to shoot for
that. We'll reconvene for what appears to be our final day at
9:00 a.m. tomorrow. We will have all morning to complete this
witness's testimony. My best guess is that we would reconvene
after lunch and we'll have the evidentiary arguments as we spoke
about yesterday, and then we will follow with the closing
arguments by counsel in the afternoon.

MR. ROTHSCHILD: Your Honor, one question.
What is your plan or ascertation for the order of closing
arguments?

MR. ROTHSCHILD: I think my understanding it
was my burden, and I was not planning on rebuttal, but that I
would go second.

THE COURT: No, I would allow you to reserve
for rebuttal if you want, but the way I see it you'd go first and
I'll allow you to reserve time for rebuttal. I think that's
appropriate under the circumstances for the plaintiff to do that,
but I think you ought to go first, I agree with Mr. Thompson in
that regard, and then we'll hear from the defendant, defendants,
and then if you want to carve out part of your time for suitable
rebuttal, and you're aware of, if you're not Liz will tell you
how much time you have left out of the hour that each side
appropriated for your openings, closings, and in the case of the
plaintiff the rebuttal, there will be one rebuttal as to the
plaintiff. If we didn't make that clear before, that's the way we
should do it. All right? Anything further?